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Published online January 9, 2008
Diabetes Care 31:770-775, 2008
DOI: 10.2337/dc07-1525
© 2008 by the American Diabetes Association
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Cardiovascular and Metabolic Risk
Original Research

Racial Disparity in Glucagon-Like Peptide 1 and Inflammation Markers Among Severely Obese Adolescents

Pedro A. Velásquez-Mieyer, MD1, Patricia A. Cowan, PHD2, Sylvia Pérez-Faustinelli, MD1, Ramfis Nieto-Martínez, MD, MSC3, Cesar Villegas-Barreto, MD1, Elizabeth A. Tolley, PHD4, Robert H. Lustig, MD5 and Bruce S. Alpert, MD1

1 Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee
2 Department of Nursing, University of Tennessee Health Science Center, Memphis, Tennessee
3 Department of Physiology, Universidad Centro-Occidental "Lisandro Alvarado," Barquisimeto, Venezuela
4 Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
5 Department of Pediatrics, University of San Francisco, San Francisco, California

Address correspondence and reprint requests to Pedro Velásquez-Mieyer, MD, Pediatrics, Le Bonheur Children’s Medical Center, 50 North Dunlap, Memphis, TN 38103. E-mail: pvelasquez{at}utmem.edu

OBJECTIVE—Compared with Caucasians, obese African-American adolescents have a higher risk for type 2 diabetes. Subclinical inflammation and reduced glucagon-like peptide 1 (GLP-1) concentration are linked to the pathogenesis of the disease. We determined the relationship between insulin resistance, β-cell activity, and subclinical inflammation with GLP-1 concentrations and whether racial disparities in GLP-1 response were present in 49 obese adolescents (14 ± 3 years; 76% African American; 71% female).

RESEARCH DESIGN AND METHODS—Subjects underwent physical examination and an oral glucose tolerance test. We measured levels of high-sensitivity CRP (CRPhs), fibrinogen, glucose, GLP-1total, GLP-1active, and insulin. Insulin and glucose area under the curve (AUC), insulinogenic index ({Delta}I30/{Delta}G30), and composite insulin sensitivity index (CISI) were computed. Subjects were categorized by race and as inflammation positive (INF+) if CRPhs or fibrinogen were elevated.

RESULTS—No racial differences were seen in mean or relative BMI. Thirty-five percent of subjects had altered fasting or 2-h glucose levels (African American vs. Caucasian, NS), and 75% were INF+ (African American vs. Caucasian, P = 0.046). Glucose and insulin, CISI, and {Delta}I30/{Delta}G30 values were similar; African Americans had lower GLP-1total AUC (P = 0.01), GLP-1active at 15 min (P = 0.03), and GLP-1active AUC (P = 0.06) and higher fibrinogen (P = 0.01) and CRPhs (NS) compared with Caucasians.

CONCLUSIONS—African Americans exhibited lower GLP-1 concentrations and increased inflammatory response. Both mechanisms may act synergistically to enhance the predisposition of obese African Americans to type 2 diabetes. Our findings might be relevant to effective deployment of emerging GLP-1–based treatments across ethnicities.

Abbreviations: AUC, area under the curve • CVD, cardiovascular disease • CISI, composite insulin sensitivity index • CRPhs, high-sensitivity C-reactive protein • DPP-IV, dipeptidyl peptidase IV • EIA, enteroinsular axis • GLP-1, glucagon-like peptide 1 • {Delta}I30/{Delta}G30, insulinogenic index • IGM, impaired glucose metabolism • IFG, impaired fasting glucose • IGT, impaired glucose tolerance • INF+, inflammation positive • NGT, normal glucose tolerance • OGTT, oral glucose tolerance test • RBMI, relative BMI • RIA, radioimmunoassay


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